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Overexpression of IBIN (CG44404) using C564-GAL4 driver enhances a group of Toll pathway target genes and shows effects on metabolism

ABSTRACT: We performed whole transcriptome profiling of adult flies overexpressing IBIN (Induced By INfection, CG44404) construct with the C564-GAL4 driver and control flies (IBIN;w1118) with and without infection with eiher E. cloacae (6h) or M. luteus (24h). Expression of a group of Toll pathway target genes upon M. luteus infection is slightly elevated when IBIN is overexpressed compared to controls. Importantly, cluster analysis of up- and downregulated genes in C564>IBIN flies without infection revealed two major gene clusters, both of which are involved in metabolism. 8/45 upregulated genes upon IBIN overexpression belong to a carbohydrate metabolism/glycoside hydrolase gene cluster, and 6/21 downregulated genes belong to a proteolysis / peptidase S1 gene cluster. Genes that had a normalized read number >10 in the treatment of interest and an expression fold change >2 were included in the cluster analysis performed with DAVID Bioinformatics resources 6.8 (https://david.ncifcrf.gov) online tool.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE120437 | GEO | 2019/01/01

REPOSITORIES: GEO

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lncRNA-CR46018 as a positive regulator controls Drosophila Toll immune response by interacting with Dif/Dorsal  

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Project description:Transcriptome profiling of immune-responsive genes in Drosophila melanogaster during Gram-positive bacterial infection was performed. The most highly induced gene by Micrococcus luteus infection was a novel gene CG44404, named Induced by Infection (IBIN). In the Flybase release FB2019_4 (22.8.2019) IBIN is annotated as coding for a short peptide. In the transcriptome analysis, fourteen immune-inducible long non-coding RNA (lncRNA) genes (Fold Change > 3) were also found.

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Dynamic miRNA-mRNA regulations are essential for maintaining Drosophila immune homeostasis during Micrococcus luteus infection

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Project description:Human African trypanosomiasis (HAT) is a protozoal disease transmitted by bites of tsetse flies. Infection with trypanosomes can lead directly to active HAT or latent infection with no detectable parasites, which may progress to active HAT or to spontaneous self-cure. Genetic variation could explain these differences in the outcome of infection. To test this hypothesis, 96 polymorphisms in 17 candidate genes were tested for association with phenotype in a case control design. The genes tested were: APOL1, CFH, HLA-A, HPR, HP, IL1B, IL12B, IL12RB1, IL10, IL4R, MIF ,TNFA, IL6, IL4, IL8, IFNG, and HLA-G.

| EGAS00001004365 | EGA

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